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fimbriae have the potential to be a virulence factor involved in colonization of
the urinary tract. However, there has been no experimental infection conducted
to demonstrate the importance of F1C fimbriae during a urinary tract infection.
S fimbriae
S fimbriae are encoded by 15% of UPEC isolates as compared to 5% fecal
E. coli strains, and are highly associated with cystitis and ABU isolates
( Spurbeck et al., 2011 ). Genetically identical to F1C fimbriae, with exception
of the tip adhesin, S fimbriae are often grouped with F1C fimbriae in epide-
miological studies ( Ott et al., 1988 ). However, the difference in the tip adhesin
between F1C and S fimbriae confers different binding specificities; thus, these
similar fimbriae should be considered different virulence factors for UPEC
( Marre et al., 1990 ). SfaS, the tip adhesin, binds sialic acid present on epithelial
cells in the human kidney ( Morschhauser et al., 1990 ), and can be inhibited
by addition of the receptor analog sialyl(α2-3)lactose ( Korhonen et al., 1986 ).
Specifically, S fimbriae bind to vascular endothelium in the large vessels of
kidney tissue and the capillary endothelium in the interstitium and glomerulus.
S fimbriae also bind to the epithelium in the lumen of the proximal and distal
tubules, the collecting ducts, and the glomerular epithelium ( Korhonen et al.,
1986 ). In the bladder, S fimbriae bind to the epithelial and muscular layers as
well as connective tissue ( Virkola et al., 1988 ). In a rat model of pyelonephritis,
deletion of a region of the chromosome that encodes hemolysin, S fimbriae,
and serum resistance from the pyelonephritis isolate E. coli 536 attenuated the
mutant. When the mutant was complemented with a plasmid containing the sfa
operon, the number of bacteria recovered from the kidneys of infected rats was
increased 20-fold ( Marre et al., 1986 ). Thus, S fimbriae fulfill the criteria of a
virulence determinant in UPEC.
F9 fimbriae
F9 fimbriae (encoded by the f9 operon) are encoded by 78% of UPEC isolates as
compared to 56% fecal E. coli strains ( Spurbeck et al., 2011 ). Although F9 fim-
briae do not agglutinate red blood cells from human, dog, horse, or sheep, nor
promote adherence to HeLa epithelial cells, this fimbria mediates biofilm for-
mation in M9 minimal salts medium when expressed in a non-fimbriated strain
of E. coli ( Ulett et al., 2007a ). However, when the f9 operon was deleted from
E. coli CFT073, no significant difference in biofilm formation was observed,
even when type 1 fimbriae and F1C fimbriae, which have been implicated in
biofilm formation, were also deleted from the chromosome ( Ulett et al., 2007a ).
Thus, F9 fimbriae play, at most, a minor role in biofilm formation by UPEC on
abiotic surfaces. F9 fimbriae are expressed when E. coli CFT073 is cultured in
human urine, which may indicate that these fimbriae have some role in viru-
lence ( Spurbeck et al., 2011 ). However, the role of F9 fimbriae in vivo or on
adherence to uroepithelial cells has not been assessed.
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